Central angiotensin induction of fetal brain c-fos expression and swallowing activity

2001 ◽  
Vol 280 (6) ◽  
pp. R1837-R1843 ◽  
Author(s):  
Zhice Xu ◽  
Calvario Glenda ◽  
Linda Day ◽  
Jiaming Yao ◽  
Michael G. Ross
Keyword(s):  
Body Fluid ◽  
Drinking Behavior ◽  
Fetal Brain ◽  
Cellular Responses ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Fluid Regulation ◽  
Fos Expression ◽  
Near Term

The present study examined physiological and cellular responses to central application of ANG II in ovine fetuses and determined the fetal central ANG-mediated dipsogenic sites in utero. Chronically prepared near-term ovine fetuses (130 ± 2 days) received injection of ANG II (1.5 μg/kg icv). Fetuses were monitored for 3.5 h for swallowing activity, after which animals were killed and fetal brains were perfused for subsequent Fos staining. Intracerebroventricular ANG II significantly increased fetal swallowing in near-term ovine fetuses (1.1 ± 0.2 to 4.5 ± 1.0 swallows/min). The initiation of stimulated fetal swallowing activity was similar to the latency of thirst responses (drinking behavior) elicited by central ANG II in adult animals. ANG II evoked increased Fos staining in putative dipsogenic centers, including the subfornical organ, organum vasculosum of the lamina terminalis, and median preoptic nucleus. Intracerebroventricular injection of ANG II also caused c- fos expression in the fetal hindbrain. These results indicate that an ANG II-mediated central dipsogenic mechanism is intact before birth, acting at sites consistent with the dipsogenic neural network. Central ANG II mechanisms likely contribute to fetal body fluid and amniotic fluid regulation.

Intravenous angiotensin induces brain c-fos expression and vasopressin release in the near-term ovine fetus

2003 ◽  
Vol 285 (6) ◽  
pp. E1216-E1222 ◽  
Author(s):  
Lijun Shi ◽  
Fang Hu ◽  
Paul Morrissey ◽  
Jiaming Yao ◽  
Zhice Xu
Keyword(s):  
Intravenous Infusion ◽  
Fetal Brain ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Double Labeling ◽  
Vasopressin Release ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Fos Expression ◽  
Near Term

The effect of intravenous angiotensin II (ANG II) on fetal brain c- fos expression and arginine vasopressin (AVP) release was studied in the near-term ovine fetus. Fetuses with chronically implanted catheters received an intravenous infusion of ANG II or saline. Fetal plasma AVP concentrations were significantly increased after the peripheral administration of ANG II, with peak levels (3-fold) at 30 min after the intravenous infusion. There was no change in fetal plasma osmolality, sodium, and hematocrit levels between the control and experimental groups or between the periods before and after the infusion of ANG II. Intravenous ANG II administration induced Fos immunoreactivity (Fos-IR) in the circumventricular organs and the median preoptic nucleus of the fetal brain. Fos-IR was also demonstrated in the fetal supraoptic nuclei (SON). Double labeling demonstrated that the AVP-containing neurons in the SON were expressing c- fos in response to intravenous ANG II. These results indicate that the peripheral ANG II in the fetus may play a significant role in stimulating the central hypothalamic-neurohypophysial system during late gestation. It supports the hypothesis that circulating ANG II may act at the fetal AVP neurons in the hypothalamus in body fluid balance via the circumventricular organs, which are situated outside the blood-brain barrier, and the central neural pathway between these two brain structures has been relatively established in utero, at least at near-term.

Median preoptic nucleus ablation does not affect angiotensin II-induced hypertension

1986 ◽  
Vol 251 (1) ◽  
pp. H148-H152
Author(s):  
G. D. Fink ◽  
C. A. Bruner ◽  
M. L. Mangiapane
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Base Line ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Water Excretion ◽  
Median Preoptic Nucleus ◽  
Induced Hypertension

Previous studies implicated the ventral median preoptic nucleus (MNPOv) in cardiovascular responses to circulating and intracerebroventricular angiotensin II (ANG II) and in normal cardiovascular and fluid homoeostasis. In the present experiments, chronically catheterized rats received continuous (24 h/day) intravenous infusions of ANG II (10 ng/min) for 5 days, and changes in mean arterial pressure, heart rate, water intake and urinary electrolyte and water excretion were determined daily. Three groups of rats were compared as follows: 1) sham-operated control rats (n = 12), 2) rats with 20-70% of the MNPOv ablated electrolytically (n = 6), and 3) rats with over 90% of the MNPOv ablated (n = 5). The organum vasculosum of the lamina terminalis was intact in all three groups. Base-line values of all measured variables were identical in the three groups on two control days preceding ANG II infusion and on two recovery days after infusion. During the administration of ANG II for 5 days, mean arterial pressure rose significantly (and similarly) in all three groups of rats; no other variable was significantly affected by ANG II infusion. These results suggest that neural pathways originating in, or passing through, the MNPOv region are not critical in the pathogenesis of ANG II-induced hypertension in the rat.

Effects of central oxytocin receptor blockade on water and saline intake, mean arterial pressure, and c-Fos expression in rats

2003 ◽  
Vol 285 (6) ◽  
pp. R1331-R1339 ◽  
Author(s):  
Douglas A. Fitts ◽  
Simon N. Thornton ◽  
Alexandra A. Ruhf ◽  
Dannielle K. Zierath ◽  
Alan Kim Johnson ◽  
...  
Keyword(s):  
Pressor Response ◽  
Inhibitory Effect ◽  
Salt Appetite ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Organum Vasculosum Laminae Terminalis ◽  
Fos Expression ◽  
Oxytocinergic Neurons ◽  
Oxytocin Antagonist ◽  
First Time

Central injection of ANG II has been proposed to have dual effects on salt appetite including a direct stimulatory effect and an indirect inhibitory effect through an activation of central oxytocinergic neurons. The inhibition was demonstrated by pretreating rats with central ornithine vasotocin (OVT; oxytocin antagonist) 30 min before a central ANG II injection. The OVT pretreatment produced a large increase in ANG II-induced saline intake. The present paper reports a failure to replicate that influential experiment. However, we also report for the first time that OVT by itself: 1) provokes drinking of both water and saline solution with a latency almost as short as that produced by ANG II; 2) produces a mild pressor response; and 3) increases c-Fos expression in the organum vasculosum laminae terminalis (OVLT) and the median preoptic nucleus (MnPO). Oxytocin activity may provide an inhibitory control of drinking responses as has been suggested, but the inhibition is tonic and includes both water and saline drinking. Inhibition of this tonic activity may stimulate drinking by increasing neural activity in the OVLT and MnPO.

Increased angiotensin II receptors in brain nuclei of DOCA-salt hypertensive rats

1988 ◽  
Vol 255 (3) ◽  
pp. H646-H650 ◽  
Author(s):  
J. S. Gutkind ◽  
M. Kurihara ◽  
J. M. Saavedra
Keyword(s):  
Angiotensin Ii ◽  
Area Postrema ◽  
Experimental Hypertension ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Salt Treatment ◽  
Brain Nuclei ◽  
Median Preoptic Nucleus ◽  
Wistar Kyoto

We analyzed angiotensin II (ANG II) receptors by in vitro autoradiography in selective brain nuclei of control, salt-treated (1% NaCl in drinking water), deoxycorticosterone acetate (DOCA)-treated (DOCA pivalate, 25 mg/kg sc weekly), and DOCA-salt-treated (DOCA + salt treatments) uninephrectomized male Wistar-Kyoto rats. After 4 wk of treatment, only the DOCA-salt group developed hypertension. ANG II binding increased in median preoptic nucleus and subfornical organ of salt- and DOCA-treated rats. DOCA-treated rats also showed increased ANG II binding in paraventricular nucleus. DOCA-salt-treated rats showed higher ANG II binding in nucleus of the solitary tract and area postrema, as well as in the areas mentioned before. Although salt and/or DOCA treatments alone increased ANG II receptors in some brain nuclei, after combined DOCA-salt treatment there was significantly higher ANG II binding in all areas, except the median preoptic nucleus. These results suggest that increased ANG II receptors in selected brain areas may play a role in the pathophysiology of mineralocorticoid-salt experimental hypertension.

Dissociation of experimentally induced drinking behavior by ibotenate injection into the median preoptic nucleus

1991 ◽  
Vol 554 (1-2) ◽  
pp. 153-158 ◽  
Author(s):  
J. Thomas Cunningham ◽  
Margaret J. Sullivan ◽  
Gaylen L. Edwards ◽  
Roxanna Farinpour ◽  
T.G. Beltz ◽  
...  
Keyword(s):  
Drinking Behavior ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Experimentally Induced

scholarly journals In utero hypoxia altered Ang II-induced contraction via PKCβ in fetal cerebral arteries

2020 ◽  
Vol 244 (1) ◽  
pp. 213-222
Author(s):  
Hongyu Su ◽  
Xueyi Chen ◽  
Yueming Zhang ◽  
Linglu Qi ◽  
Yun He ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cerebral Circulation ◽  
Cerebral Arteries ◽  
Fetal Brain ◽  
Calcium Transient ◽  
In Utero ◽  
Protective Effects ◽  
Ang Ii ◽  
Voltage Dependent ◽  
Near Term

Cerebral circulation is important in fetal brain development, and angiotensin II (Ang II) plays vital roles in regulation of adult cerebral circulation. However, functions of Ang II in fetal cerebral vasculature and influences of in utero hypoxia on Ang II-mediated fetal cerebral vascular responses are largely unknown. This study investigated the effects and mechanisms of in utero hypoxia on fetal middle cerebral arteries (MCA) via Ang II. Near-term ovine fetuses were exposed to in utero hypoxia, and fetal MCA responses to Ang II were tested for vascular tension, calcium transient, and molecular analysis. Ang II caused significant dose-dependent contraction in control fetal MCA. Ang II-induced MCA constriction was decreased significantly in hypoxic fetuses. Neither losartan (AT1R antagonist, 10−5 mol/L) nor PD123,319 (AT2R antagonist, 10−5 mol/L) altered Ang II-mediated contraction in fetal MCA. Phenylephrine-mediated constriction was also significantly weaker in hypoxic fetuses. Bay K8644 caused similar contractions between the two groups. Protein expression of L-type voltage-dependent calcium channels was unchanged. There were no differences in caffeine-mediated vascular tension or calcium transients. Contraction induced by PDBu (PKC agonist) was obviously weaker in hypoxic MCA. Protein expression of PKCβ was reduced in the hypoxic compared with the control, along with no differences in phosphorylation levels. The results showed that fetal MCA was functionally responsive to Ang II near term. Intrauterine hypoxia reduced the vascular agonist-mediated contraction in fetal MCA, probably via decreasing PKCβ and its phosphorylation, which might play protective effects on fetal cerebral circulation against transient hypoxia.

Comparison of fos-like immunoreactivity induced in rat brain by central injection of angiotensin II and carbachol

1994 ◽  
Vol 267 (3) ◽  
pp. R792-R798 ◽  
Author(s):  
N. E. Rowland ◽  
B. H. Li ◽  
A. K. Rozelle ◽  
G. C. Smith
Keyword(s):  
Angiotensin Ii ◽  
Ang Ii ◽  
Angiotensin Receptor ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Immunocytochemical Detection ◽  
Organum Vasculosum Laminae Terminalis ◽  
Hypothalamic Nuclei ◽  
At1 Antagonist ◽  
Intracerebroventricular Injections

Rats were given intracerebroventricular injections of either angiotensin II (ANG II) or the cholinomimetic carbachol. Some rats received cotreatment with ANG II antagonists selective for either angiotensin receptor AT1 (losartan) or AT2 (PD-123319, CGP-42112A). One hour later, the rats were killed and the brains processed for immunocytochemical detection of Fos-like immunoreactivity (FLI). ANG II treatment induced strong FLI in the anterior subfornical organ (SFO), median preoptic nucleus (MnPO), organum vasculosum laminae terminalis (OVLT), and supraoptic and paraventricular hypothalamic nuclei (SON, PVH). The AT1 antagonist abolished FLI in all regions normally stimulated by ANG II. The AT2 antagonist PD-123319 reduced FLI in SON and PVH, but CGP-42112A was less effective. Carbachol induced strong FLI in SON, PVH, and MnPO and only moderate FLI in SFO and OVLT. The AT1 antagonist prevented carbachol-induced FLI in the MnPO only. The distributions of FLI are compared between these central dipsogens and with that previously reported after peripheral infusion of ANG II, and their implications for mapping central thirst pathways are discussed.

scholarly journals Inactivation of median preoptic nucleus causes c-Fos expression in hypocretin- and serotonin-containing neurons in anesthetized rat

2008 ◽  
Vol 1234 ◽  
pp. 66-77 ◽  
Author(s):  
Sunil Kumar ◽  
Ronald Szymusiak ◽  
Tariq Bashir ◽  
Natalia Suntsova ◽  
Seema Rai ◽  
...  
Keyword(s):  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Fos Expression

The median preoptic nucleus: front and centre for the regulation of body fluid, sodium, temperature, sleep and cardiovascular homeostasis

2015 ◽  
Vol 214 (1) ◽  
pp. 8-32 ◽  
Author(s):  
M. J. McKinley ◽  
S. T. Yao ◽  
A. Uschakov ◽  
R. M. McAllen ◽  
M. Rundgren ◽  
...  
Keyword(s):  
Body Fluid ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Cardiovascular Homeostasis

Osmotic threshold and sensitivity for vasopressin release and Fos expression by hypertonic NaCl in ovine fetus

2000 ◽  
Vol 279 (6) ◽  
pp. E1207-E1215 ◽  
Author(s):  
Zhice Xu ◽  
Calvario Glenda ◽  
Linda Day ◽  
Jiaming Yao ◽  
Michael G. Ross
Keyword(s):  
Fetal Brain ◽  
Plasma Osmolality ◽  
Ang Ii ◽  
Double Labeling ◽  
Fetal Sheep ◽  
Vasopressin Release ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Near Term ◽  
Stimulation Of

In adults, hyperosmolality stimulates central osmoreceptors, resulting in arginine vasopressin (AVP) secretion. Near-term fetal sheep have also developed mechanisms to respond to intravascular hypertonicity with stimulation of in utero AVP release. However, prior studies demonstrating fetal AVP secretion have utilized plasma tonicity changes greater than those required for adult osmotically induced AVP stimulation. We sought to examine near-term fetal plasma osmolality threshold and sensitivity for stimulation of AVP secretion and to correlate plasma hormone levels with central neuronal responsiveness. Chronically instrumented ovine fetuses (130 ± 2 days) and maternal ewes simultaneously received either isotonic or hypertonic intravascular NaCl infusions. Maternal and fetal plasma AVP and angiotensin II (ANG II) levels were examined at progressively increasing levels of plasma hypertonicity. Intravenous hypertonic NaCl gradually elevated plasma osmolality and sodium levels. Both maternal and fetal plasma AVP increased during hypertonicity, whereas ANG II levels were not changed. Maternal AVP levels significantly increased with a 3% increase in plasma osmolality, whereas fetal plasma AVP significantly increased only at higher plasma osmolality levels (over 6%). Thus the slope of the regression of AVP vs. osmolality was greater for ewes than for fetuses (0.232 vs. 0.064), despite similar maternal and fetal plasma osmolality thresholds for AVP secretion (302 vs. 304 mosmol/kg). Hyperosmolality induced Fos immunoreactivity (FOS-ir) in the circumventricular organs of the fetal brain. FOS-ir was also demonstrated in the fetal supraoptic and paraventricular nuclei (SON and PVN), and double labeling demonstrated that AVP-containing neurons in the SON and PVN expressed Fos in response to intravenous NaCl. These results demonstrate that, in the ovine fetus at 130 days of gestation, neuroendocrine responses to cellular dehydration are functional, although they evidence a relatively reduced sensitivity for AVP secretion compared with the adult.

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